Dr. Molnár Ildikó 2010-ben megjelent könyve

Dr. Molnár Ildikó PhD. 2010-ben megjelent angol nyelvű könyvének rövid kivonatát alább találja:

Nervous, Immune, Endocrine Regulatory Systems and Diseases Associated with Nerve Growth Factor Co-Secretion

Ildikó Molnár

Immunoendocrinology, EndoMed, 4032 Debrecen, Bem tér 18/C., Hungary


Nerve growth factor (NGF) plays an essential role in the cellular interactions as a member of neurotrophins via controlling the balance between the cell survival and apoptosis, as well as in the differentiation of the motor and sensory neurons. The excessive cell survival may promote the onset of cancers and autoimmune diseases, but the insufficient cell survival could contribute to tissue degeneration and the development of several diseases. Besides of its neuronal origin, NGF is also involved in the inflammatory and immune processes. The cells of the innate and adaptive immune systems are able to secret NGF and bear receptors for NGF. The cytokines that are released from the activated immune cells, influence the activities of the central and peripheral nervous systems. As a growth factor for the sympathetic nervous system, NGF is involved in the catecho­lamine release by the activation of the hypothalamic-pituitary-adrenal axis. The glands, adipose tissue, muscles, skin and orbital tissues are highly sympathetically innervated organs. Due to the increased sympathoadrenal activity and the immune responses, NGF could be respected as a regulatory factor among the neural, inflammatory, immune and hormonal processes. The auto­immune endocrine diseases reflect a complexity of the neuro-immune-endocrine activities associating with hypertrophy and cardiovascular damages.

The NGF-specific receptor activation via tyrosine kinase (TrkA) differs from the activations induced by hormones and other growth factors, which exhibit mainly G protein-mediated protein kinase activations. Much data have been reported on a cross-talk or transactivation of the NGF receptors with the adrenergic or G protein-coupled receptors, which could be demon­strated in the receptor signaling mechanisms of the different receptor-mediated activations. The receptor p75NTR is involved in the regulation of the programmed cell death during the neurogenesis and the NGF withdrawal.

The main NGF secreting cells are the mast cells, eosinophils, monocytes, lymphocytes, fibroblasts, the smooth muscle and endothelial cells. These cells not only secret NGF but also bear its receptors playing a central role in the inflammatory, allergic and immune diseases. Some of these cells possess receptors for corticotropin-releasing hormone (CRH) and adrenergic receptors. The enhanced sympathoadrenal activity and the catecholamine release thereby may contribute to the activation of these cells resulting in a cytokine release. The cytokines and the NGF interactions can modify the immune reactions leading to a T helper 2 dominance, acting towards the direction of cell survival.

The increased adrenergic receptor activity is responsible for the hypertrophy of the glands, the adipose and muscle tissues. NGF plays a role in the interaction between the target cells and the axon terminals of sympathetic and sensory neurons. On another way, NGF as a trophic factor increases the density of the sympathetic innervation and the adrenergic receptor expression. The increased catecholamine levels induce a resistance to insulin, thereby contributing to the damage of the muscle cells and adipocytes. The catecholamine cytotoxicity and the chronic stimulation of the adrenergic receptors lead to the tissue hypertrophy and an increase in the sympathetic neuron apoptosis. The NGF stimulated angiogenetic effect associates with the hypertrophy and the severity of atherosclerosis. A transactivation between the adenosine and the TrkA receptor activations have been demonstrated after tissue injury caused by hypoxia.

In brief, NGF exerts a relevant role in the tissue repair via improving the sympathetic innervation, the cell survival mechanisms and the inflammatory and immunocompetent cell activations.

The endocrine diseases, particularly the autoimmune disorders, respresent a network of the neural, hormonal and immune processes. The hormones associating with the increased cate­cholamine release and the enhanced sympathoadrenal activity could contribute to the T helper 2 dominance, the tissue hypertrophy and the cardiovascular damage. It is no doubt that NGF is involved in the development of cardiac diseases, inducing hypertrophy through its modulating effects. The thyroid hormones promote the trophical effect of NGF via the transduction of the cell survival signal. An increased activation of the hypothalamic-pituitary-adrenal axis could be detected in diabetes mellitus. The damages of the adipose and muscle tissues exhibit a complexity of the neural, hormonal and immuno-inflammatory networks. It seems that the trophical effects of several growth factors and the durable stimulation of the adrenergic receptors may associate with the tissue hypertrophy and the enhanced apoptosis. The deterioration of the sympathetic and sensory innervations affects a wide spectrum of the tissues causing thyroid, diabetes and other endocrine diseases. The overloaded sympatho­adrenal activity and the other chronic stimulating factors also affect the cardiovascular tissues. It seems that this affection can not be avoided. Early revealing of the endocrine dysfunctions should be the most important for the prevention of the cardiovascular diseases.

The neural, hormonal, inflammatory and immune processes form a network not only at the tissue levels but also at the cellular levels. NGF plays a modulatory role in this network and contributes to the best homeostasis of the patients.


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